Glucose metabolism disorder: a potential accomplice of SARS-CoV-2

被引:7
作者
Luan, Yi [1 ]
Luan, Ying [2 ]
He, Hongbo [3 ]
Jue, Bolin [4 ]
Yang, Yang [1 ]
Qin, Bo [1 ]
Ren, Kaidi [5 ,6 ]
机构
[1] Zhengzhou Univ, Dept Translat Med Ctr, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China
[2] Peking Univ, Sch Phys, State Key Lab Artificial Microstruct & Mesoscop Ph, Beijing 100000, Peoples R China
[3] Zhengzhou Univ, Dept Thorac Surg, Affiliated Hosp 1, Zhengzhou 450001, Peoples R China
[4] Xinxiang Med Univ, Sch Basic Med Sci, Xinxiang 453000, Peoples R China
[5] Zhengzhou Univ, Dept Pharm, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China
[6] Zhengzhou Univ, Henan Key Lab Precis Clin Pharm, Zhengzhou 450052, Peoples R China
基金
中国国家自然科学基金;
关键词
COVID-19; RECEPTOR; CELLS; EXPRESSION; INHIBITORS; INFECTION; LEPTIN; GP73;
D O I
10.1038/s41366-023-01352-y
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Globally, 265,713,467 confirmed cases of SARS-CoV-2 (CoV-2), including 5,260,888 deaths, have been reported by the WHO. It is important to study the mechanism of this infectious disease. A variety of evidences show the potential association between CoV-2 and glucose metabolism. Notably, people with type 2 diabetes mellitus (T2DM) and other metabolic complications were prone to have a higher risk of developing a more severe infection course than people who were metabolically normal. The correlations between glucose metabolism and CoV-2 progression have been widely revealed. This review will discuss the association between glucose metabolism disorders and CoV-2 progression, showing the promoting effect of diabetes and other diseases related to glucose metabolism disorders on the progression of CoV-2. We will further conclude the effects of key proteins and pathways in glucose metabolism regulation on CoV-2 progression and potential interventions by targeting glucose metabolism disorders for CoV-2 treatment. Therefore, this review will provide systematic insight into the treatment of CoV-2 from the perspective of glucose metabolism.
引用
收藏
页码:893 / 902
页数:10
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